Translational Neurodegeneration,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: Dec. 6, 2024
Abstract
Extracellular
vesicles
(EVs)
are
membrane
originating
from
different
cells
within
the
brain.
The
pathophysiological
role
of
EVs
in
neurodegenerative
diseases
is
progressively
acknowledged.
This
field
has
advanced
basic
biological
research
to
essential
clinical
significance.
capacity
selectively
enrich
specific
subsets
biofluids
via
distinctive
surface
markers
opened
new
avenues
for
molecular
understandings
across
various
tissues
and
organs,
notably
In
recent
years,
brain-derived
have
been
extensively
investigated
as
biomarkers,
therapeutic
targets,
drug-delivery
vehicles
diseases.
review
provides
a
brief
overview
characteristics
physiological
functions
classes
EVs,
focusing
on
mechanisms
by
which
types
mediate
occurrence
development
Concurrently,
novel
approaches
challenges
use
delivery
delineated.
Parkinson's
disease
(PD)
is
a
degenerative
neurological
condition
marked
by
the
gradual
loss
of
dopaminergic
neurons
in
substantia
nigra
pars
compacta.
The
precise
etiology
PD
remains
unclear,
but
emerging
evidence
suggests
significant
role
for
disrupted
autophagy-a
crucial
cellular
process
maintaining
protein
and
organelle
integrity.
Biomolecules,
Journal Year:
2023,
Volume and Issue:
13(10), P. 1435 - 1435
Published: Sept. 22, 2023
Parkinson’s
disease
(PD)
is
a
devastating
associated
with
accumulation
of
α-synuclein
(α-Syn)
within
dopaminergic
neurons,
leading
to
neuronal
death.
PD
characterized
by
both
motor
and
non-motor
clinical
symptoms.
Several
studies
indicate
that
autophagy,
an
important
intracellular
degradation
pathway,
may
be
involved
in
different
neurodegenerative
diseases
including
PD.
The
autophagic
process
mediates
the
protein
aggregates,
damaged
unneeded
proteins,
organelles,
allowing
their
clearance,
thereby
maintaining
cell
homeostasis.
Impaired
autophagy
cause
abnormal
proteins.
Incomplete
or
impaired
explain
neurotoxic
aggregates
several
Indeed,
have
suggested
contribution
α-Syn
accumulation,
death
neuroinflammation.
In
this
review,
we
summarize
recent
literature
on
involvement
pathogenesis.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
25(1), P. 360 - 360
Published: Dec. 26, 2023
Parkinson’s
disease
(PD)
is
a
complex
neurodegenerative
characterized
by
the
progressive
loss
of
dopaminergic
neurons
in
substantia
nigra
and
widespread
accumulation
alpha-synuclein
(αSyn)
protein
aggregates.
αSyn
aggregation
disrupts
critical
cellular
processes,
including
synaptic
function,
mitochondrial
integrity,
proteostasis,
which
culminate
neuronal
cell
death.
Importantly,
pathology
extends
beyond
neurons—it
also
encompasses
spreading
throughout
environment
internalization
microglia
astrocytes.
Once
internalized,
glia
can
act
as
neuroprotective
scavengers,
limit
spread
αSyn.
However,
they
become
reactive,
thereby
contributing
to
neuroinflammation
progression
PD.
Recent
advances
research
have
enabled
molecular
diagnosis
PD
accelerated
development
targeted
therapies.
Nevertheless,
despite
more
than
two
decades
research,
mechanisms,
induction
damage
remain
incompletely
understood.
Unraveling
interplay
between
αSyn,
neurons,
may
provide
insights
into
initiation
progression,
bring
us
closer
exploring
new
effective
therapeutic
strategies.
Herein,
we
an
overview
recent
studies
emphasizing
multifaceted
nature
its
impact
on
both
neuron
glial
damage.
Frontiers in Molecular Neuroscience,
Journal Year:
2024,
Volume and Issue:
17
Published: March 11, 2024
Exosomes,
vesicular
structures
originating
from
cells,
participate
in
the
conveyance
of
proteins
and
nucleic
acids.
Presently,
centrality
epigenetic
modifications
neurological
disorders
is
widely
acknowledged.
Exosomes
exert
influence
over
various
phenomena,
thereby
modulating
post-transcriptional
regulatory
processes
contingent
upon
their
constituent
makeup.
Consequently,
heightened
attention
directed
toward
exosomes
as
instigators
alterations
has
burgeoned
recent
years.
Notably,
serve
vehicles
for
delivering
methyltransferases
to
recipient
cells.
More
significantly,
non-coding
RNAs,
particularly
microRNAs
(miRNAs),
represent
pivotal
contents
within
exosomes,
wielding
capacity
expression
diverse
factors
cerebral
milieu.
The
transfer
these
exosomal
amidst
brain
encompassing
neuronal
cells
microglia,
assumes
a
critical
role
genesis
progression
disorders,
also,
this
not
limited
it
may
deal
with
any
human
disease,
such
cancer,
cardiovascular
diseases.
This
review
will
concentrate
on
elucidating
regulation
exosome-induced
events
its
subsequent
ramifications
A
more
profound
comprehension
involvement
exosome-mediated
contributes
awareness
etiology
advancement
afflictions.
Ageing and Neurodegenerative Diseases,
Journal Year:
2025,
Volume and Issue:
5(1)
Published: March 18, 2025
Autophagy
is
a
cellular
process
essential
for
maintaining
neuronal
homeostasis
by
degrading
and
recycling
damaged
organelles
proteins.
Impairments
in
canonical
autophagy
pathways,
such
as
macroautophagy,
chaperone-mediated
(CMA),
mitophagy,
are
linked
to
Parkinson’s
disease
(PD)
pathogenesis,
contributing
α-synuclein
aggregation
dopaminergic
loss.
Moreover,
the
recent
discovery
of
noncanonical
highlights
unexpected
roles
autophagy-related
proteins
protein
degradation
beyond
pathways.
Advances
understanding
molecular
mechanisms
provide
potential
therapeutic
strategies
modulate
this
pathway
PD.
Key
targets
include
mTOR
AMPK,
with
compounds
like
rapamycin,
trehalose,
resveratrol
showing
promise
preclinical
models.
Enhancing
lysosomal
function
mitophagy
also
presents
viable
strategy
alleviate
PD
symptoms.
This
review
emphasizes
complex
modulation
promising
treating
disease.
Journal of Extracellular Vesicles,
Journal Year:
2024,
Volume and Issue:
13(12)
Published: Dec. 1, 2024
Abstract
The
application
of
extracellular
vesicles
(EVs)
as
vehicles
for
anti‐Parkinson's
agents
represents
a
significant
advance,
yet
their
clinical
translation
is
hampered
by
challenges
in
efficient
brain
delivery
and
complex
blood‐brain
barrier
(BBB)
targeting
strategies.
In
this
study,
we
engineered
dopamine
onto
the
surface
adipose‐derived
stem
cell
EVs
(Dopa‐EVs)
utilizing
facile,
two‐step
cross‐linking
approach.
This
engineering
enhanced
neuronal
uptake
primary
neurons
neuroblastoma
cells,
process
shown
to
be
competitively
inhibited
pretreatment
receptor
antibodies.
Notably,
Dopa‐EVs
demonstrated
increased
accumulation
mouse
Parkinson's
disease
(PD)
models.
Therapeutically,
administration
led
rescue
dopaminergic
loss
amelioration
behavioural
deficits
both
6‐hydroxydopamine
(6‐OHDA)
α‐Syn
PFF‐induced
PD
Furthermore,
observed
that
stimulated
autophagy
evidenced
upregulation
Beclin‐1
LC3‐II.
These
findings
collectively
indicate
modification
with
presents
potent
strategy
brain.
remarkable
therapeutic
potential
Dopa‐EVs,
models,
positions
them
highly
promising
candidate
treatment,
offering
advance
over
current
modalities.
Cellular and Molecular Life Sciences,
Journal Year:
2024,
Volume and Issue:
81(1)
Published: May 1, 2024
Abstract
Glial
cells
constitute
nearly
half
of
the
mammalian
nervous
system's
cellular
composition.
The
glia
in
C.
elegans
perform
majority
tasks
comparable
to
those
conducted
by
their
equivalents.
cephalic
sheath
(CEPsh)
glia,
which
are
known
be
counterparts
astrocytes,
enriched
with
two
nuclear
hormone
receptors
(NHRs)—NHR-210
and
NHR-231.
This
unique
enrichment
makes
CEPsh
these
NHRs
intriguing
subjects
study
concerning
neuronal
health.
We
endeavored
assess
role
neurodegenerative
diseases
related
functional
processes,
using
transgenic
expressing
human
alpha-synuclein.
employed
RNAi-mediated
silencing,
followed
behavioural,
functional,
metabolic
profiling
relation
suppression
NHR-210
231.
Our
findings
revealed
that
depleting
nhr-210
changes
dopamine-associated
behaviour
mitochondrial
function
alpha
synuclein-expressing
strains
NL5901
UA44,
through
a
putative
target,
pgp-9
,
transmembrane
transporter.
Considering
alteration
involvement
transporter,
we
performed
metabolomics
via
HR-MAS
NMR
spectroscopy.
Remarkably,
substantial
modifications
ATP,
betaine,
lactate,
glycine
levels
were
seen
upon
absence
.
also
detected
considerable
pathways
such
as
phenylalanine,
tyrosine,
tryptophan
biosynthesis
metabolism;
glycine,
serine,
threonine
well
glyoxalate
dicarboxylate
metabolism.
In
conclusion,
deficiency
receptor
alpha-synuclein
strain
results
altered
function,
coupled
alterations
vital
metabolite
levels.
These
underline
physiological
importance
glia.
Graphical
abstract
